ArticleeLife2023
Myoglobin-derived iron causes wound enlargement and impaired regeneration in pressure injuries of muscle.
Article in eLife, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Who cites it
6 citing papers in PubMed, 10 citations in OpenAlex.
- Modulation of Macrophage ferroptosis under the guide of infrared thermography promotes the healing of pressure injuries.Journal of advanced research · 2026Article
- Ischemia/reperfusion-associated oxidative stress is an aggravating factor for pressure ulcers.Journal of clinical biochemistry and nutrition · 2025Article
- The emerging role and therapeutical implications of ferroptosis in wound healing.Burns & trauma · 2025Review
- SAT1/ALOX15 Signaling Pathway Is Involved in Ferroptosis After Skeletal Muscle Contusion.International journal of molecular sciences · 2024Article
- Quantification of muscle fiber malformations using edge detection to investigate chronic muscle pressure ulcers.Frontiers in bioinformatics · 2024Article
- Myoglobin-derived iron causes wound enlargement and impaired regeneration in pressure injuries of muscle.eLife · 2023Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The reasons for poor healing of pressure injuries are poorly understood. Vascular ulcers are worsened by extracellular release of hemoglobin, so we examined the impact of myoglobin (Mb) iron in murine muscle pressure injuries (mPI). Tests used Mb-knockout or treatment with deferoxamine iron chelator (DFO). Unlike acute injuries from cardiotoxin, mPI regenerated poorly with a lack of viable immune cells, persistence of dead tissue (necro-slough), and abnormal deposition of iron. However, Mb-knockout or DFO-treated mPI displayed a reversal of the pathology: decreased tissue death, decreased iron deposition, decrease in markers of oxidative damage, and higher numbers of intact immune cells. Subsequently, DFO treatment improved myofiber regeneration and morphology. We conclude that myoglobin iron contributes to tissue death in mPI. Remarkably, a large fraction of muscle death in untreated mPI occurred later than, and was preventable by, DFO treatment, even though treatment started 12 hr after pressure was removed. This demonstrates an opportunity for post-pressure prevention to salvage tissue viability.
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Registered trials
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